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Neuromuscular junction

Chemical Transmission of an action potential across a


synapse
Action potential arrives at presynaptic neurone
1. Voltage gated Ca2+ channels open
2. Ca2+ diffuses into presynaptic cleft causes vesicles to move
and fuse with plasma membrane
3. Acetylcholine released by exocytosis
Synthesized from choline and acetyl CoA
Uses enzyme choline acetyltransferase
4. Acetylcholine diffuses across the gap
5. Bind to receptors on postsynaptic neurone
Receptors are made from 5 glycoprotein
subunits 2 , , ,
Lipophilic parts of the proteins point
outwards so the pore can sit in the
membrane
Hydrophilic negatively charged amino acids
point inwards so only cations can pass
through
chains have acetylcholine binding sites
Both need to be occupied for the pore to
open
Stops small Ach causing receptor to open
Can be desensitized receptors stop opening after repeated
stimulation
6. Na+ and K+ diffuse into the postsynaptic cleft excitatory
postsynaptic current (EPSC)
The diffusing of lots of monovalent ions though all the
receptors causes an end plate potential (EPP) as PD becomes
less negative
As more and more ions diffuse in, the current gets smaller
7. Current will dissipate into cell body
If its large enough an action potential is generated
8. End plate potential EPP peaks in postsynaptic cleft
Tends to reversal (Nernst) potential of 0mV
9. Acetylcholine is broken into choline and acetic acid
Uses enzyme acetylcholine esterase
What other factors could cause miniature end plate potentials?
Random small influxes of current
Decreased external calcium
Increased external potassium
Increased osmotic pressure

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